Bilateral white matter abnormality in children with frontal lobe epilepsy.

In frontal lobe epilepsy (FLE), interictal discharges and seizures are more likely to spread to contralateral hemisphere and become secondarily generalized. The aim of this study was to assess white matter (WM) integrity in children with FLE using diffusion tensor imaging (DTI). Children with FLE and normal MRI, and healthy controls with no neurological or psychiatric disorders underwent DTI on 3T MRI. Whole brain fractional anisotropy (FA) and mean diffusivity (MD) maps were compared between right and left FLE with controls. 43 children with FLE, consisting of 28 left and 15 right FLE, and 44 healthy controls were recruited. Patients with left FLE had significant FA reductions in left (p=0.002) and right (p=0.003 and p=0.034) superior longitudinal fasciculi (SLF), genu/body (p=0.0002) and splenium (p=0.011) of corpus callosum. Patients with right FLE had significant FA reductions in left (p=0.016) and right (p=0.033) SLF, genu (p=0.001) and body of corpus callosum (p=0.001 and p=0.008), and significant MD elevation in right thalamus (p=0.032). There was no significant association between FA or MD and clinical seizure parameters. The abnormal WM both ipsilateral and contralateral to seizure focus may be due to seizure activity or abnormal brain development.

Systematic protocol for assessment of the validity of BOLD MRI in a rabbit model of inflammatory arthritis at 1.5 tesla.

BACKGROUND: Blood-oxygen-level-dependent (BOLD) MRI has the potential to identify regions of early hypoxic and vascular joint changes in inflammatory arthritis. There is no standard protocol for analysis of BOLD MRI measurements in musculoskeletal disorders. OBJECTIVE: To optimize the following BOLD MRI reading parameters: (1) statistical threshold values (low, r > 0.01 versus high, r > 0.2); (2) summary measures of BOLD contrast (percentage of activated voxels [PT%] versus percentage signal difference between on-and-off signal intensities [diff_on_off]); and (3) direction of BOLD response (positive, negative and positive + negative). MATERIALS AND METHODS: Using BOLD MRI protocols at 1.5 T, arthritic (n = 21) and contralateral (n = 21) knees of 21 juvenile rabbits were imaged at baseline and on days 1, 14 and 28 after a unilateral intra-articular injection of carrageenan. Nine non-injected rabbits served as external control knees (n = 18). By comparing arthritic to contralateral knees, receiver operating characteristic curves were used to determine diagnostic accuracy. RESULTS: Using diff_on_off and positive + negative responses, a threshold of r > 0.01 was more accurate than r > 0.2 (P = 0.03 at day 28). Comparison of summary measures yielded no statistically significant difference (P > 0.05). Although positive + negative (AUC = 0.86 at day 28) and negative responses (AUC = 0.90 at day 28) for PT% were the most diagnostically accurate, positive + negative responses for diff_on_off (AUC = 0.78 at day 28) also had acceptable accuracy. CONCLUSIONS: The most clinically relevant reading parameters included a lower threshold of r > 0.01 and a positive + negative BOLD response. We propose that diff_on_off is a more clinically relevant summary measure of BOLD MRI, while PT% can be used as an ancillary measure.

Short- and long-term plasticity of eye position information: examining perceptual, attentional, and motor influences on perisaccadic perception.

Spatial vision requires information about eye position to account for eye movements. But integrating eye position information and information about objects in the world is imperfect and can lead to transient misperceptions around the time of saccadic eye movements most likely because the signals are prone to temporal errors making it difficult to tell when the retinas move relative to when retinal images move. To clarify where this uncertainty comes from, in four experiments we examined influences of eye posture, attentional cueing, and trial history on perisaccadic misperceptions. We found evidence for one longer-term modulation of perisaccadic shift that evolved over the time of the test session due to biased eye posture. Another, short-term influence on perisaccadic shift was related to eye posture during preceding trials or the direction of the preceding saccade. Both perceptual effects could not be explained with visual delays, influences of attention or changes in saccade metrics. Our data are consistent with the idea that perisaccadic shift is caused by neural representations of eye position or space that are plastic and that arise from non-motor, extraretinal mechanisms. This suggests a perceptual system that continuously calibrates itself in response to changes in oculomotor and muscle systems to reconstruct a stable percept of the world.